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66 results for “novel pathogens”
Simulated NGS datasets for real-time detection of novel pathogens
<p>Datasets based on the <a href="https://doi.org/10.5281/zenodo.3678563">bacterial</a> and <a href="https://doi.org/10.5281/zenodo.4312525">viral</a> simulated NGS datasets. Fastq files correspond to tests sets of those datasets. Basecall files were generated based on the fastq files with an 8nt simulated barcode between the mates of a read pair. The "rn" datasets containg random length subreads (25-250bp) of the original validation and training reads.</p> <p>The Nanopore datasets were resimulated with <a href="https://github.com/liyu95/DeepSimulator">DeepSimulator 1.5</a> (Li et al., 2020) based on the original datasets (i.e. using the same species composition as the original data). The test Nanopore dataset contains full reads (target average length: 8kb) and the training and validation datasets - 250bp subreads.</p>
Simulated NGS read datasets for prediction of novel fungal pathogens and multiple pathogen classes
<p>This repository contains simulated Illumina read datasets for novel fungal pathogen prediction and real-time detection of multiple pathogen classes. They were used to train the models hosted at <a href="https://zenodo.org/record/5711877">https://zenodo.org/record/5711877</a>.<br> The reads were simulated with Mason (<a href="https://www.seqan.de/apps/mason/">https://www.seqan.de/apps/mason/</a>) from genomes downloaded from NCBI, based on metadata stored in a manually curated database (<a href="https://zenodo.org/record/5846345">https://zenodo.org/record/5846345</a>).</p> <p>We provide the following:</p> <p>1) An rds file describing assignment of fungal species from the database (<a href="https://zenodo.org/record/5846345">https://zenodo.org/record/5846345</a>) to training, validation and test sets (TrainValTest_fungi.rds). A second rds file (TrainValTest_temporal.rds) includes species added within 12 weeks after the original datasets were compiled. Those species were used for a temporal benchmark.</p> <p>2) Fungal validation and test sets. Each contains 1.25 million, 250bp-long reads simulated from non-overlapping sets of human ("pathogenic") or non-human ("nonpathogenic") pathogens. The test set contains paired reads ("_1" and "_2" for the first and second mate). The number of reads per species is proportional to the respective genome length. An additional, temporal test set (*temporal*fasta.gz) includes 15 species added after 12 weeks from the consturction of the original datasets.</p> <p>3) Fungal training sets. They contain 250bp-long reads simulated from species not present in the validation or test sets. There are four variants:<br> 3a) "low-coverage, linear" - 20 million reads, number of reads per species proportional to genome length<br> 3b) "low-coverage, logarithmic" - 20 million reads, number of reads per species proportional to the logarithm of genome length ("log")<br> 3c) "high-coverage, linear" - 240 million reads, number of reads per species proportional to genome length ("24")<br> 3d) "high-coverage, logarithmic" - 240 million reads, number of reads per species proportional to the logarithm of genome length ("24log")</p> <p>4) Training, validation and test sets for the multiclass models. They should be used together with the "pathogenic" read sets hosted at <a href="https://zenodo.org/record/4456857">https://zenodo.org/record/4456857</a>. Here, we share sets for two of the four total classes:<br> 4a) The 'non-pathogen' class is a mixture of "nonpathogenic" biacterial and viral read sets, concatenated and downsampled to the original read number (20M for training, 1.25M for validation and test). The training and validation sets contain mixed-length (25-20bp) simulated subreads (original sets hosted here: <a href="https://zenodo.org/record/4456857">https://zenodo.org/record/4456857</a>). The test set contains 250bp long reads based on the test sets from here: <a href="https://zenodo.org/record/3678563">https://zenodo.org/record/3678563</a> and here: <a href="https://zenodo.org/record/4312525">https://zenodo.org/record/4312525</a>; it was also sorted by species.<br> 4b) Mixed-length versions of the "pathogenic" fungal training and validation sets, prepared by random shortening of the "low-coverage" read sets in the "linear" (_rn_) and "logarithmic" (_rn_*log_) flavours.</p> <p>See also the preprint: <a href="https://www.biorxiv.org/content/10.1101/2021.11.30.470625">https://www.biorxiv.org/content/10.1101/2021.11.30.470625</a></p>
Defining the genes required for survival of Mycobacterium bovis in the bovine host offers novel insights into the genetic basis of survival of pathogenic mycobacteria
<p>Supplementary dataset from "<strong><em>Defining the genes required for survival of Mycobacterium bovis in the bovine host offers novel insights into the genetic basis of survival of pathogenic mycobacteria</em></strong>"</p> <p> </p> <p><strong>Supplementary Figure legends</strong></p> <p><strong>Figure S1. Illustration of the transposon insertions around the <em>M. bovis </em>genome. </strong>Sequencing of the input library showed that transposon insertions were evenly distributed around the genome and 27,419 of the permissible 66,931 thymine–adenine dinucleotide (TA) sites contained an insertion representing an insertion density of ~41%. The outer ring are the genomic coordinates, the blue lines represent transposon insertions and the gray boxes indicate regions of that did not have any insertions. Plot made with Circlize (Gu et al, 2014).</p> <p> </p> <p><strong>Figure S2. Diversity of the output library isolated from lung and thoracic lymph node lesions compared to the input library. </strong>On average, libraries recovered from lung lesions contained 14,456 unique mutants and those recovered from the lymph nodes contained an average of 16,210 unique mutants. Insertion density is represented as a proportion of the TA sites that contained insertions. The numbers on the x-axis refer to the sequencing file from that sample and come from individual animals (Bioproject ID: PRJNA816175, Submission ID: SUB11067380).</p> <p> </p> <p><strong>Figure S3. Volcano plots showing the distribution of log<sub>2</sub> fold-changes and -log<sub>10</sub> of adjusted p-values for representative lung (A) and lymph node (B) samples. </strong>Adjusted p-values (BH-fdr correction) < 0.000001 cluster at the limits of the plot and precision reflects the number of resampling iterations (10,000).</p> <p> </p> <p><strong>Figure S4. Scatterplot of mean log<sub>2</sub> fold change per gene for all lung samples against all thoracic lymph node samples</strong>. Correlation between mean log<sub>2</sub> fold change among genes between the tissues was calculated with Spearman's ranked correlation, = 0.878, p-value < 2.2e-16.</p> <p> </p> <p><strong>Figure S5. Fold-changes caused by transposon insertions in <em>RD1<sup>BCG</sup></em> and <em>RD1<sup>MIC</sup> </em>in the lungs and lymph nodes of infected cattle. </strong>Boxplot for log<sub>2 </sub>fold-changes in genes of the RD1<sup>BCG</sup> region. Samples with adjusted p-values (BH-fdr corrected) <0.05 are indicated with purple points. Gene names highlighted in magenta have fewer than 5 TA sites located in the gene; too few to determine the statistical significance of changes in insertion levels with this method.</p> <p> </p> <p><strong>Supplementary Tables </strong></p> <p><strong>Table S1. Sequencing statistics of the input and output transposon libraries. </strong>The numbers in the column labelled “filename” refers to the sequencing file from that sample and come from individual animals (Bioproject ID: PRJNA816175, Submission ID: SUB11067380).</p> <p> </p> <p><strong>Table S2. Tissues collected and scored for gross pathology. </strong>Tissues from head and neck lymph nodes (from the right and left sub-mandibular lymph nodes, the right and left medial retropharyngeal lymph nodes), thoracic lymph nodes (the right and left bronchial lymph nodes, the cranial tracheobronchial lymph nodes, the cranial and caudal mediastinal lymph nodes) and from lung lesions, were collected and scored.</p> <p> </p> <p><strong>Table S3. Log<sub>2</sub> fold-changes for insertions across the entire genome of <em>M. bovis</em> AF2122/97. </strong>Cells are coloured according to log<sub>2</sub> fold-change. Refer to the text for the gene groups in individual tabs.</p> <p> </p> <p><strong>Table S4. </strong>Custom transposon sequencing primers and adaptors used in sequencing of the transposon libraries.</p> <p> </p>
SUPPLEMENTARY (For MD) An integrative pan-genome and subtractive proteomics approach for the identification of potential novel therapeutic drug target against antibiotic resistant honeybee pathogen Paenibacillus larvae
<p><strong>Parameters</strong></p><p>Force field: AMBER ff19SB</p><p>Water type: TIP3P</p><p>Ions: NaCl </p><p>Ligand topology force field: GAFF2</p><p>Temperature: 298k</p><p>Pressure: 1 bar</p><p>minimization step: 20000 on 5 nanoseconds</p><p>initial velocity is changed by changing "ntx" and "ig"</p><p>C2: ntx = 5 , ig = 8</p><p>C3: ntx = 2 , ig = 5</p><p> </p><p><strong>Uploads</strong>- </p><p>1. Zip file of all 3 main files</p><p>2. Unzip file of C1 (Trajectory, PDB complex after each 10 ns run, and Mp4 video of Complex)</p><p>3. Zip file of C1</p><p>4. Unzip file of C2 (Trajectory, PDB complex after each 10 ns run, and Mp4 video of Complex)</p><p>5. Zip file of C2</p><p>6. Unzip file of C3 (Trajectory, PDB complex after each 10 ns run, and Mp4 video of Complex)</p><p>7. Zip file of C3</p><p>8. Zip and unzip file of <strong>Initial</strong> PDB of complex prior to MD simulation with <strong>Post</strong> MD PDB (C1, C2, C3)</p><p>9. Zip file of <strong>topology</strong> files for C1, C2, and C3</p>
Code and data for: Are novel or locally adapted pathogens more devastating and why? : resolving opposing hypotheses
<p>The naive host syndrome hypothesis suggests that pathogens are able to easily invade and become deadly to novel hosts because of a lack of co-evolutionary history, whereas the local adaptation hypothesis suggests that pathogens are better able to invade local hosts because of their co-evolutionary history, but rarely do studies on these two hypotheses cite one another or acknowledge their ostensibly mixed messages. By combining a continental-scale, factorial, common garden experiment with a global-scale meta-analysis, each on the amphibian-chytrid fungus host-pathogen system, we show that local host-pathogen interactions typically resulted in higher host mortality, greater infection success, and higher pathogen loads, but that there was substantial variation in novel host-pathogen outcomes and thus moving pathogens around the planet increases the likelihood of exposure to particularly virulent pathogen strains and particularly deadly host-pathogen combination. Therefore, we provide support for both the local adaptation and naïve host syndrome hypotheses, highlight how the two hypotheses are complementary rather than conflicting, and emphasize the need for greater integration of these hypotheses and their associated semi-disparate literature.</p>
Reference data from the Pathomove simulation, for the manuscript "Novel pathogen introduction triggers rapid evolution in animal social movement strategies"
<p>This is a reference dataset of multiple runs of the 'Pathomove' simulation, to accompany the manuscript "Novel pathogen introduction rapidly alters the evolution of movement, restructuring animal societies". The datasets are in the form of R data objects saved as Rds files.</p> <p>This version of the data is intended to accompany a resubmission to <em>eLife</em>.</p>
Perturbations in fatty acid metabolism and collagen production infer pathogenicity of a novel MBTPS2 variant in Osteogenesis imperfecta
<p>(i) PCR-sequencing: Chromatograms were generated by PCR-sequencing of a region within exon 4 of MBTPS2 using DNA extracted from a healthy control and the proband's fibroblasts</p> <p>(ii) Gene expression was quantified by qRT-PCR using RNA extracted from fibroblasts. Transcript levels of each gene of interest was calculated using the 2^-deltaCt method with normalization to the average Ct values of endogenous control genes GAPDH, IPO8 and TBP.</p> <p>(iii) Cellular fatty acid content was quantified by GC-MS/MS. Each table represents one technical replicate. Absolute values of each fatty acid are listed in the tables; relative ratios of various fatty acids are calculated at the bottom of each table. </p> <p>(iv) Immunocytochemistry images of ECM proteins (COL1 = collagen type I; COL4 = collagen type IV; COL5 = collagen type V; a2b1 = integrin a2b1) and binding of collagen-hybridising peptide (R-CHP).</p>
Code and data for: Are novel or locally adapted pathogens more devastating and why? : resolving opposing hypotheses
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Novel multiplex TaqMan assay for differentiation of the four major pathogenic Brachyspira species in swine
<p>Table S1</p> <p>503 Brachyspira samples used for validation of the novel 5-plex qPCR assay and comparison of results obtained by four independent PCR assays</p>
Data for: Rapid adaptation to a novel pathogen through disease tolerance in a wild songbird
<p class="MsoNormal"><span>Animal hosts can adapt to emerging infectious disease through both disease resistance, which decreases pathogen numbers, and disease tolerance, which limits damage during infection without limiting pathogen replication. Both resistance and tolerance mechanisms can drive pathogen transmission dynamics. However, it is not well understood how quickly host tolerance evolves in response to novel pathogens or what physiological mechanisms underlie this defense. Using natural populations of house finches (<em>Haemorhous mexicanus</em>) across the temporal invasion gradient of a recently emerged bacterial pathogen (<em>Mycoplasma gallisepticum</em>), we find rapid evolution of tolerance (<25 years). In particular, populations with a longer history of MG endemism have less pathology but similar pathogen loads compared with populations with a shorter history of MG endemism. Further, gene expression data reveal that more targeted immune responses early in infection are associated with tolerance. These results suggest an important role for tolerance in host adaptation to emerging infectious diseases, a phenomenon with broad implications for pathogen spread and evolution. </span></p>
Data from: A novel molecular toolkit for rapid detection of the pathogen and primary vector of thousand cankers disease
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Data from: Genetic independence of naturally correlated variation in resistance to endemic and novel pathogens
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Data from: Experimental adaptation to singular pathogen challenge reduces susceptibility to novel pathogens in Drosophila melanogaster
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Data for: Rapid adaptation to a novel pathogen through disease tolerance in a wild songbird
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Data from: Adaptive variation for growth and resistance to a novel pathogen along climatic gradients in a foundation tree
Natural ecosystems are under pressure from increasing abiotic and biotic stressors, including climate change and novel pathogens, which are putting species at risk of local extinction, and altering community structure, composition, and function. Here, we aim to assess adaptive variation in growth and fungal disease resistance within a foundation tree, Corymbia calophylla to determine local adaptation, trait heritability, and genetic constraints in adapting to future environments. Two experimental planting sites were established in regions of contrasting rainfall with seed families from 18 populations capturing a wide range of climate origins (~4000 individuals at each site). Every individual was measured in 2015 and 2016 for growth (height, basal diameter) and disease resistance to a recently introduced leaf blight pathogen (Quambalaria pitereka). Narrow-sense heritability was estimated along with trait covariation. Trait variation was regressed against climate-of-origin and multivariate models were used to develop predictive maps of growth and disease resistance. Growth and blight resistance traits differed significantly among populations, and these differences were consistent between experimental sites and sampling years. Growth and blight resistance were heritable, and comparisons between trait differentiation (QST) and genetic differentiation (FST) revealed that population differences in height and blight resistance traits are due to divergent natural selection. Traits were significantly correlated with climate-of-origin, with cool and wet populations showing the highest levels of growth and blight resistance. These results provide evidence that plants have adaptive growth strategies and pathogen defense strategies. Indeed, the presence of standing genetic variation and trait heritability of growth and blight resistance provide capacity to respond to novel, external pressures. The integration of genetic variation into adaptive management strategies, such as assisted gene migration and seed sourcing, may be used to provide greater resilience for natural ecosystems to both biotic and abiotic stressors.
Contrasting impacts of a novel specialist vector on multi-host viral pathogen epidemiology in wild and managed bees
<p>Typically pathogens infect multiple host species. Such multi-host pathogens can show considerable variation in their degree of infection and transmission specificity, which has important implications for potential disease emergence. Transmission of multi-host pathogens can be driven by key host species and changes in such transmission networks can lead to disease emergence. We study two viruses that show contrasting patterns of prevalence and specificity in managed honeybees and wild bumblebees, black queen cell virus (BQCV) and slow bee paralysis virus (SBPV), in the context of the novel transmission route provided by the virus-vectoring <i>Varroa destructor</i>. Our key result is that viral communities and RNA virus genetic variation are structured by location, not host species or <i>V. destructor</i> presence. Interspecific transmission is pervasive with the same viral variants circulating between pollinator hosts in each location; yet, we find virus-specific host differences in prevalence and viral load. Importantly, <i>V. destructor </i>presence increases the prevalence in honeybees and, indirectly, in wild bumblebees, but in contrast to its impact on deformed wing virus (DWV), BQCV and SBPV viral loads are not increased by <i>Varroa </i>presence, and do not show genetic evidence of recent emergence. Effective control of <i>Varroa</i> in managed honeybee colonies is necessary to mitigate further disease emergence, and alleviate disease pressure on our vital wild bee populations. More generally, our results highlight the over-riding importance of geographical location to the epidemiological outcome despite the complexity of multi-host-parasite interactions.</p>
Data from: Adaptive potential of ash (Fraxinus excelsior) populations against the novel emerging pathogen Hymenoscyphus pseudoalbidus
An emerging infectious pathogen Hymenoscyphus pseudoalbidus has spread across much of Europe within recent years causing devastating damage on European common ash trees (Fraxinus excelsior) and associated plant communities. The present study demonstrates the presence of additive genetic variation in susceptibility of natural F. excelsior populations to the new invasive disease. We observe high levels of additive variation in the degree of susceptibility with relatively low influence of environmental factors (narrow sense heritability = 0.37-0.52). Most native trees are found highly susceptible, and we estimate that only around 1% has the potential of producing offspring with expected crown damage of less than 10% under the present disease pressure. The results suggest that the presence of additive genetic diversity in natural F. excelsior populations can confer the species with important ability to recover, but that low resistance within natural European populations is to be expected due to a low frequency of the hypo-sensitive trees. Large effective population sizes will be required to avoid genetic bottlenecks. The role of artificial selection and breeding for protection of the species is discussed based on the findings.
Two novel Trichoderma species and their antagonistic activity against sclerotia-producing plant pathogens
<p>Alignments used to reconstruct the phylogenetic trees in the manuscript.</p>
Data from: Ultrafast evolution and loss of CRISPRs following a host shift in a novel wildlife pathogen, Mycoplasma gallisepticum
Measureable rates of genome evolution are well documented in human pathogens but are less well understood in bacterial pathogens in the wild, particularly during and after host switches. Mycoplasma gallisepticum (MG) is a pathogenic bacterium that has evolved predominantly in poultry and recently jumped to wild house finches (Carpodacus mexicanus), a common North American songbird. For the first time we characterize the genome and measure rates of genome evolution in House Finch isolates of MG, as well as in poultry outgroups. Using whole genome sequences of 12 House Finch isolates across a 13-year serial sample and an additional four newly sequenced poultry strains, we estimate a nucleotide diversity in House Finch isolates of only ~2% of ancestral poultry strains and a nucleotide substitution rate of 0.8 – 1.2 X 10-5 per site per year both in poultry and in House Finches, an exceptionally fast rate rivaling some of the highest estimates reported thus far for bacteria. We also found high diversity and complete turnover of CRISPR arrays in poultry MG strains prior to the switch to the House Finch host, but after the invasion of House Finches, there is progressive loss of CRISPR repeat diversity, and recruitment of novel CRISPR repeats ceases. Recent (2007) House Finch MG strains retain only ~50% of the CRISPR repertoire founding (1994-95) strains and have lost the CRISPR-associated genes required for CRISPR function. Our results suggest that genome evolution in bacterial pathogens of wild birds can be extremely rapid and in this case is accompanied by apparent functional loss of CRISPRs.
Comprehensive genomic analysis identifies a diverse landscape of sideroblastic and non-sideroblastic iron related anemias with novel and pathogenic variants in an iron deficient endemic setting
<p>The history for the 5 CMA cases are as follows:-</p> <p> </p> <p>1. <strong>HMA-2 </strong>:- 0.6 month male child presented with poor feeding and noted to have mild-moderate pallor. CBC showed Hemoglobin 9.0gm/dl, MCV- 58fl, MCH 17.3, MCHC 29, Iron 113 ug/dl, Ferritin 297 ug/l, TSAT-45%, TIBC-297 ug/dl, Hepcidin- 20.3ng/ml. No transfusions received and antenatal and neonatal history uneventful. HPLC (both parents), alpha sequencing normal. Targeted NGS shows a heterozygous VUS in GLRX5 gene along with a VUS in BMP6 gene. WES- Does not add anything further significant.</p> <p> </p> <p>2. <strong>HMA-3 </strong>:- 0.8 month male child with transfusion dependent microcytic hypochromic anemia and neurological developmental delay. Expired at 1 year of age due to secondary infection (acinetobacter and toxoplasmosis). Hb- 6.5, MCV-61.5, MCH-18.3, Iron 45 ug/dl, Ferritin 650. Targeted panel and WES - negative.</p> <p> </p> <p>3. <strong>HMA-4:</strong>- 5 year male child with severe microcytic hypochromic anemia and received just one transfusion outside. Has microcephaly and SNHL. Hb 5, MCV- 56, MCH- 18, MCHC- 23, Iron- 75, Ferritin - 330, TIBC- 290, TSAT- 41%. Targeted NGS and WES show a Homozygous VUS in BMP6 gene (? association?) </p> <p> </p> <p>4. <strong>HMA-6:-</strong> 2 year old male child with moderate microcytic hypochromic anemia and focal seizures. Hb -8, MCV- 58, MCH- 16, MCHC-27, Iron- 94, Ferritin -380, Transferrin levels- 10 (very low). Targeted NGS and WES show a single heterozygous VUS mutation in TF gene and another intrinsic rare variant but reported in pop. Database (could it make it compound her for atransferrinemia?) </p> <p> </p> <p>5. <strong>HMA-7:-</strong> 7 year male child with short stature, consanguinity in family, moderate macrocytic anemia with HB-7, MCV-113, Iron-55, Ferritin -209, TSAT-54%. Also Bone marrow shows coarse vacuolations in erythroid cells (12%) and 19% RS. Suspicion PMS- But MLPA for mitochondrial genome normal, no deletions. Targeted panel NGS and WES reveal a heterozygous VUS in LARS2 gene (? nature).</p> <p> </p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.